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Biology Of Ageing Year2 > DNA damage and repair > Flashcards

DNA damage and repair Flashcards

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1
Q

What are human progeria syndromes?

A

Mutations lead to increased DNA damage
and/or failure to repair damage this then leads to premature ageing.

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2
Q

How much DNA damage is present in each cell?

A

19,200

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3
Q

How much DNA damage is there in the whole body?

A

710,000

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4
Q

What are the sources of DNA damage?

A

Metabolism
UV light
Ionising radiation
DNA synthesis
Environmental mutagens

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5
Q

What are ROS?

A

Reactive oxygen species

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6
Q

Where do the reactive oxygen species come from?

A

Produced by every cell during metabolism in the mitochondria.

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7
Q

What is the problem with 8-oxodG being in the body??

A

Causes pairing so bad DNA replication.

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8
Q

How does UV lead to DNA damage?

A

Produces pyrimidine dimers in exposed tissue, these replicate single strand breaks which cause double strand breaks which are toxic.

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9
Q

How does ionising radiation cause DNA damage?

A

Directly causes double-strand breaks which is the most toxic damage?

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10
Q

What is a manmade ionising radiation?

A

Cancer treatment

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11
Q

What wave range is UV light?

A

300nm

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12
Q

Where does ionising radiation come from?

A

Radon
Cosmic rats
Radionucleotides

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13
Q

How does DNA synthesis lead to DNA damage?

A

It is highly error-prone and DNA strand breaks occur.

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14
Q

How many mistakes occur per replicated genome?

A

600

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15
Q

What are environmental mutagens?

A

Food
Water
Air-borne
Smoking
Industrial

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16
Q

How do cells cope with DNA damage?

A

DNA repair
They prevent the replication of damaged DNA, apoptosis kills damaged cells.

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17
Q

What is MGMT?

A

O-6-methylguanine-DNA which is a DNA damage repair protein.

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18
Q

Why isn’t MGMT an enzyme?

A

It can only function once.

19
Q

What is the direct role of MGMT?

A

Repairs methylation damage.

20
Q

What does global genome NER mean?

A

Involving the whole genome.

21
Q

What does T-coupled NER mean?

A

Involving the transcription complex part of the genome.

22
Q

What is NER?

A

Nucleotide excision repair

23
Q

What is nucleotide excision repair?

A

The primary mechanism for repair of UV induced
damage (XP).

24
Q

What is the difference between the global NER and t-coupled NER pathways?

A

Proteins which recognise damage.

25
Q

Which proteins recognise damage during t-coupled NER pathways?

A

CSA and CSB.

26
Q

Which proteins recognise damage during global NER pathways?

A

XB/C

27
Q

What is C syndrome?

A

Damage to CSA/B proteins which recognise the damage in t-coupled NER.

28
Q

What does C syndrome lead to?

A

TF2H complex abnormalities (transcription factors).

29
Q

What is Xeroderma pigmentosum?

A

Leads to XB mutations.

30
Q

What is Base excision repair?

A

The main mechanism for repair of oxidative
damage. (Also alkylation, deamination,
depurination/depyrimidination)

31
Q

What kinds of base excision repair exists?

A

Short and long patch.

32
Q

When is base excision repair used?

A

During single base damage.

33
Q

What is damage recognised by during base excision repair?

A

DNA glycosylase (OOG1).

34
Q

How was it proved that DNA glycosylase is used for recognition in base excision repair?

A

Using knockout mice.

35
Q

What is mismatch repair?

A

The primary mechanism for recognition of DNA mismatches arising during DNA replication.

36
Q

What kinds of mismatch repair occurs during DNA replication?

A

– Single base mismatches
– Small insertion/deletions

37
Q

Why is mismatch repair important during cancer?

A

Recognises chemically-induced DNA damage, including important chemo-therapeutics.

38
Q

What is the risk with mutations to the mismatch repair pathway?

A

Mutations in this pathway are associated with
familial colon cancer

39
Q

Why are double strand breaks the most toxic double-strand lesions?

A

Can lead to chromosome aberrations.

40
Q

What are the 2 different mechanisms of double-strand break repair?

A

– Non-homologous end joining.
– Homologous recombination.

41
Q

What is the problem with non-homologous end joining?

A

It is highly error-prone, if ends are broken in the same place deletion occurs (however this prevents cancer).

42
Q

What is the positive of homologous recombination?

A

It is error free.

43
Q

When does homologous recombination ocuur?

A

Late S/G2.

44
Q

What is the most common solution to double stranded breaks?

A

Apoptosis.

Biology Of Ageing Year2 (23 decks)

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